In experimental liver cirrhosis, proline for collagen synthesis may be derived chiefly from glutamate. It is proposed to elucidate the enzymic mechanism of the reduction of glutamate to proline in normal and fibrotic rat liver, to quantitatively evaluate the shifts in the metabolic pathways synthesizing proline during the development of experimental liver disease and to obtain information on the physiological controls which regulate the biosynthetic pathways for proline, with respect to its availability for the synthesis of collagen. On the basis of the information obtained it is hoped that a rational chemotherapy for fibrosis may be developed.